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KEN OKAZAKI
Department School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine Position Professor and Division head |
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| Article types | Original article |
| Language | English |
| Peer review | Peer reviewed |
| Title | Alcohol consumption induces murine osteoporosis by downregulation of natural killer T-like cell activity. |
| Journal | Formal name：Immunity, inflammation and disease Abbreviation：Immun Inflamm Dis ISSN code：20504527/20504527 |
| Domestic / Foregin | Foregin |
| Volume, Issue, Page | 9(4),pp.1370-1382 |
| Author and coauthor | NRUO Munehiko, NEGISHI Yasuyuki, OKUDA Takahisa, KATSUYAMA Midori, OKAZAKI Ken, MORITA Rimpei |
| Publication date | 2021/12 |
| Summary | INTRODUCTION:Chronic alcohol consumption (CAC) can induce several deleterious effects on the body, including the promotion of osteoporosis; however, the immunological mechanism underlying alcohol-induced osteoporosis is still unclear.METHODS:We administered alcohol to mice for 4 weeks as the experimental CAC model and analyzed the bone and immune cells that are located in the vicinity of a bone.RESULTS:IL-4 is known to be a suppressive factor for osteoclastogenesis, and we found that natural killer T (NKT)-like cells, which showed NK1.1-positive, CD3-positive, and α-galactosylceramide-loaded CD1d tetramer-negative, produced IL-4 more effectively than CD4+ T and natural killer (NK) cells. The alcohol consumption facilitated a significant decrease of bone mineral density with the upregulation of nuclear factor of activated T cells 1 and receptor activator of NF-κB ligand expression. Meanwhile, we confirmed that alcohol consumption suppressed the activity of antigen-presenting cells (APCs) and NKT-like cells, leading to decreased IL-4 secretion. Moreover, these harmful effects of alcohol consumption were reduced by simultaneous treatment with a glycolipid antigen OCH.CONCLUSIONS:Our results indicate that the inactivation of innate immune cells, APCs, and NKT-like cells are likely to be crucial for alcohol-induced osteoporosis and provide a new therapeutic approach for preventing osteoporosis. |
| DOI | 10.1002/iid3.485 |
| PMID | 34214248 |